N-acetylcysteine mitigates oxidative damage to the ovary in D-galactose-induced ovarian failure in rabbits

Background Oxidative damage to the ovaries is the primary cause of impaired reproductive functions in female animals. This study aimed to investigate the protective role of N-Acetyl-L-cysteine (NAC) in reducing oxidative damage in the ovaries of female rabbits. Methods and results Female rabbit ovar...

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Published inMolecular biology reports Vol. 51; no. 1; p. 1008
Main Authors Xue, Yu, Bian, Huafeng, Bai, Shaocheng, Bao, Zhiyuan, Wang, Lei, Wang, Sen, Zhao, Bohao, Wu, Xinsheng, Chen, Yang
Format Journal Article
LanguageEnglish
Published Dordrecht Springer Netherlands 01.12.2024
Springer Nature B.V
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Summary:Background Oxidative damage to the ovaries is the primary cause of impaired reproductive functions in female animals. This study aimed to investigate the protective role of N-Acetyl-L-cysteine (NAC) in reducing oxidative damage in the ovaries of female rabbits. Methods and results Female rabbit ovaries were treated in vitro with varying concentrations of D-galactose (D-gal): 0, 5, 10, and 15 mg/mL, and it was found that 10 mg/mL D-gal significantly disrupted follicular structures, causing disarray in granulosa cell arrangements and significantly reducing T-SOD and GSH levels ( p  <  0.01 ). Consequently, we selected 10 mg/mL D-gal to establish an ovarian failure model. These models were treated with multiple doses of NAC (0, 0.1, 0.3, 0.5 mg/mL). The results revealed that the disruption in granulosa cell arrangement caused by 10 mg/mL D-gal was effectively alleviated by 0.1 mg/mL NAC compared to the D-gal treatment group. Furthermore, 10 mg/mL D-gal significantly ( p  < 0.01) reduced GSH, T-SOD, and catalase (CAT) levels in the ovaries. However, 0.1 mg/mL NAC effectively ( p  < 0.01) suppressed these adverse effects. Moreover, the current results showed that 10 mg/mL D-gal alone significantly ( p  < 0.01) downregulated the expression of Nrf2, GPX, PRDX4, GSR, SOD1 , and TAF4B , whereas 0.1 mg/mL NAC counteracted these suppressive effects ( p  < 0.01). Conclusions It could be concluded that NAC may delay ovarian failure by reducing D-gal-induced ovarian oxidative damage in female rabbit, suggested NAC could be a promising therapeutic agent for protecting against ovarian failure and potentially delaying ovarian failure in female rabbits.
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ISSN:0301-4851
1573-4978
1573-4978
DOI:10.1007/s11033-024-09951-2